WILMINGTON, Del., Oct. 19, 2021 /PRNewswire/ -- The link between Alzheimer's disease and an infection of Herpes Simplex Virus 1 (HSV-1), the most common herpes virus, is well established. But scientists still don't know if and how the virus causes the disease. This mystery is unraveled in a new scientific study authored by Dr. Hanan Polansky and Benjamin Goral from the Center for the Biology of Chronic Disease (CBCD). The study was published on Oct 11, 2021 in the Journal of NeuroVirology.

HSV-1 was previously thought to be harmless when "latent," or not causing expected symptoms associated with the virus, such as cold sores. The discovery shows that in fact HSV-1 is causing serious damage to the brain associated with Alzheimer's. The study answers many important questions, including: why only certain infected individuals develop Alzheimer's; what can be done to better diagnose the disease in these infected people; and how we can prevent the development of Alzheimer's, or even treat it? The authors used the Microcompetition Model introduced by Dr. Hanan Polansky in his book "Microcompetition and Foreign DNA and the Origin of Chronic Disease." In the book, Dr. Polansky establishes that viruses not exhibiting the expected symptoms are still causing severe diseases, such as cancer, Parkinson's, and more.

The discovery relies on observations reported in hundreds of published studies. One such study showed conclusively that individuals with an HSV-1 symptomatic infection are almost three-times more likely to develop Alzheimer's when compared to asymptomatic or uninfected individuals. HSV-1 infects a region of the brain called the hippocampus that is also susceptible to damage in Alzheimer's. Using the Microcompetition Model, the study explains how HSV-1 causes the devastating damages in the brain characteristic of Alzheimer's. HSV-1 hijacks a limiting cellular resource, and over time, causes amyloid plaque and cognitive decline. HSV-1 also hampers the brain's ability to repair the damage via neurogenesis, or the process of generating new neurons, eventually leading to Alzheimer's. Most importantly, the changes in the brain predicted by the model match the experimental results reported in dozens of autopsies from deceased Alzheimer's patients.

The study also answers the following important question: If up to 90% of the population is infected with HSV-1, why do only some people develop Alzheimer's? Polansky and Goral demonstrate that the difference between infected individuals who develop Alzheimer's and those who don't, is in their high viral copy number, and not the presence of expected symptoms, such as cold sores. Only a high enough viral concentration, or number of copies, of latent HSV-1 in the hippocampus will affect the cellular resource allocation, and, over time, lead to Alzheimer's. This realization matches published results: that using anti-herpetic medications, that are known to reduce the viral copy number, dramatically lowered the risk for dementia by five-fold. Since symptomatic patients usually harbor a greater viral copy number, this explains why they are at greater risk compared to asymptomatic or uninfected individuals.

This is the first study ever to explain how latent HSV-1 can cause Alzheimer's. The CBCD now calls for further research on this discovery. We believe that this research will lead to superior diagnostic methods and treatments for Alzheimer's that can substantially improve the health of a significant portion of the global population.

If you are interested in more information on the discovery, how you can get involved, or how you or someone you know can benefit from it, please refer this article to your doctor or contact us directly at [email protected].

Media Contact:
Mike Davis, CBCD
607-256-6070
[email protected]

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SOURCE CBCD